title: Clonidine normalizes levels of P50 gating in patients with schizophrenia on stable medication.
abstract: BACKGROUND
  Sensory gating deficits are among the core features of schizophrenia. Recently, we reported significantly increased sensorimotor gating following additional administration of single dosages of clonidine to the treatment of stably medicated patients with schizophrenia who, in spite of their medication, showed gating deficits. In the current study, we investigated whether this result is generalizable to filtering of sensory information as a whole, by examining clonidine's effect on P50 suppression in the same group of patients.
  
  
  METHODS
  In a double-blind, placebo-controlled, randomized yet balanced cross-over design, 20 male schizophrenia patients on stable medication were assessed in a psychophysiological test battery, including a sensory gating paradigm on 5 occasions: once after oral administration of placebo and after single doses of 25, 50, 75, and 150 µg of clonidine. Their results were compared with 20 age-matched healthy male volunteers, who received no treatment.
  
  
  RESULTS
  Patients showed significantly reduced levels of P50 suppression in the placebo session compared with controls. All dosages of clonidine significantly diminished these deficits to such levels that they no longer differed significantly from the healthy controls (except the highest dose).
  
  
  CONCLUSIONS
  This is the first study to show that even a single low dose of clonidine administered to stably medicated patients with schizophrenia not only significantly increases their levels of P50 suppression but also normalizes them. The results indicate that α2-noradrenergic agonists are capable of normalizing levels of P50 gating, which has a potentially high clinical relevance for the medical treatment of schizophrenia.
authors.affiliation: Center for Neuropsychiatric Schizophrenia Research (CNSR) and Center for Clinical Intervention and Neuropsychiatric Schizophrenia Research (CINS), Copenhagen University Hospital, Psychiatric Center Glostrup, Glostrup, Denmark;Faculty of Health Sciences, Department of Neurology, Psychiatry, and Sensory Sciences, University of Copenhagen, Copenhagen, Denmark B.Oranje@cnsr.dk.
authors.forename: Bob
authors.initials: B
authors.lastname: Oranje
authors.affiliation: Center for Neuropsychiatric Schizophrenia Research (CNSR) and Center for Clinical Intervention and Neuropsychiatric Schizophrenia Research (CINS), Copenhagen University Hospital, Psychiatric Center Glostrup, Glostrup, Denmark;Faculty of Health Sciences, Department of Neurology, Psychiatry, and Sensory Sciences, University of Copenhagen, Copenhagen, Denmark.
authors.forename: Birte Y
authors.initials: BY
authors.lastname: Glenthøj
mesh_terms: D058647:Adrenergic alpha-2 Receptor Agonists / Q000008:administration & dosage / Q000494:pharmacology*; D000328:Adult; D003000:Clonidine / Q000008:administration & dosage / Q000494:pharmacology*; D018592:Cross-Over Studies; D004311:Double-Blind Method; D004569:Electroencephalography; D005071:Evoked Potentials / Q000187:drug effects*; D006801:Humans; D008297:Male; D008875:Middle Aged; D012559:Schizophrenia / Q000188:drug therapy* / Q000503:physiopathology; D055139:Sensory Gating / Q000187:drug effects*; D016896:Treatment Outcome
chemical_list: D058647:Adrenergic alpha-2 Receptor Agonists; D003000:Clonidine
keywords: P50 suppression; chronic schizophrenia; clonidine; noradrenaline